Objective To investigate the relationship between smoking and lung cancer by evidence-based evaluation. Methods Using Meta-analysis method, the results of 29 case-control studies involving the relationship between smoking and lung cancer in recent decade were analyzed by Review Manager 4. 2 software. Results The association between smoking and lung cancer was significant ( Z =12. 16, P lt; 0. 000 01) , and the pooled OR value was 5. 75( 4. 34, 7. 62) . The population attributable risk percentage( PARP) of smoking was 69. 16% . The pooled OR of 1-10 cpd( cigarettes per day) , 10-20 cpd, 20-40 cpd and more than 40 cpd were 1. 97( 1. 69, 2. 30) , 5. 20( 3. 54, 7. 62) , 7. 46( 5. 22, 10. 67) and 15. 14 ( 5. 27, 43. 44) respectively. The pooled OR of less than 20 years of smoking duration, 20-40 years and more than 40 years were 1. 25( 1. 01, 1. 53) , 5. 10( 3. 03, 8. 57) and 10. 77( 7. 30, 15. 89) respectively. While the pooled ORof less than 10 pack-years, 10-20 pack-years, 20-40 pack-years and more than 40 pack-years were 1. 73( 1. 01, 2. 96) , 3. 73 ( 3. 02, 4. 61) , 5. 69 ( 3. 79, 8. 54) and 8. 41 ( 4. 56, 15. 51) respectively. The pooled OR of initial smoking age less than 15 years old, 15-20 years old and more than 20 years old were 13. 31( 7. 09, 24. 97) , 7. 21( 4. 51, 11. 52) and 4. 74( 3. 47, 6. 47) respectively. The pooled OR of quitting smoking for 1-10 years, 10-20 years and more than 20 years were 7. 16( 4. 70, 10. 91) , 2. 12( 1. 16, 3. 86)and 1. 47 ( 0. 67, 3. 20 ) respectively, and more than 20 years of quitting smoking had no significant difference. The pooled OR of light smoking and deep smoking were 3. 26( 1. 24, 8. 58) and 8. 07( 4. 67, 13. 94) respectively. Conclusions Smoking is an important risk factor of lung cancer. Meta-anlalysis revealed cigarettes comsuption per day, smoking duration, total amount of cigarettes ( pack-years) , smoking behaviour( depth) , initial age of smoking and duration of quitting smoking can increase the risk of lung cancer.
ObjectiveTo evaluate the smoking environment, its related knowledge and difference between urban and rural areas in Chengdu.
MethodsIn December 2010, we randomly sampled and investigated 60 dwellers aged from 35 to 70 from urban and rural communities, who were 1:1 paired by the age and sex. Questionnaires survey was used.
ResultsThere were 48.3% (29/60) dwellers thought that smoking should be allowed freely at home, of which 30.0% (9/30)rural homes had no rules about smoking prohibited. There were 93.3% (28/30) urban dwellers supported male smoking. About 86.7%-98.3% urban dwellers realized that many diseases such as heart disease, stroke, and lung cancer may be due to smoking. And 16.7% urban dwellers also realized that cigarettes can result in diabetes mellitus, but none of rural dwellers did. The publicity of smoking cessation among urban dwellers (91.7%) by mass media was better than rural ones (0.0%). There were 95.0% dwellers denied any institution or organization for smoking control.
ConclusionThe dwellers were short of cognition about restrictions of smoking environment and non-smoking knowledge. It's different between urban and rural area in tobacco advertisement and publicity of smoking cessation. We should continue enhancing public education, forbiding tobacco advertisement and providing institutions for smoking control.
ObjectiveTo investigate the influence of endoplasmic reticulum stress (ERS) on smoking-induced nucleus pulposus cells apoptosis and inflammatory response.MethodsBetween October 2016 and October 2018, 25 patients with cervical disc herniation receiving discectomy were collected and divided into smoking group (14 cases) and non-smoking group (11 cases). The baseline data of age, gender, herniated segment, and Pfirrmann grading showed no significant difference between the two groups (P>0.05). The obtained nucelus pulposus tissues were harvested to observe the cell apoptosis via detecting the apoptosis-related proteins (Caspase-3 and PRAP) by TUNEL staining and Western blot test. The nucleus pulposus cells were isolated and cultured with enzyme digestion, of which the third generation cells were used in follow-up experiments. Then, the expressions of inflammatory factors [interleukin 1β (IL-1β) and tumor necrosis factor α (TNF-α)] were detected by ELISA; the nuclear translocation of P65 was monitored by cell immunofluorescence staining. Furthermore, ERS-related proteins (GRP78 and CHOP) were detected by Western blot; and endoplasmic reticulum ultrastructure was observed under transmission electron microscope. To verify the regulatory effect of ERS, cells were pretreated by ERS specific inhibitor (4-PBA), then cell apoptosis and inflammatory response were tested.ResultsThe nucleus pulposus tissue observation showed that the cell apoptotic rate and the expressions of apoptosis-related proteins (Caspase-3 and PARP) were obviously higher in smoking group than in non-smoking group (P<0.05). The nucleus pulposus cells observation indicated that the expressions of the inflammatory factors (IL-1β and TNF-α) and the ERS-related proteins (GRP78 and CHOP) were also higher in smoking group than in non-smoking group (P<0.05). The results of cell immunofluorescence staining further confirmed that smoking stimulated nuclear translocation of P65 in nucleus pulposus cells. The ERS injury was much more serious in smoking group than in non-smoking group. Furthermore, after 4-PBA inhibiting ERS, the expressions of GRP78, CHOP, IL-1β, TNF-α, and P65 were significantly decreased (P<0.05), and flow cytometry results showed that cell apoptotic rate in smoking group was decreased, showing significant difference compared with the non-smoking group (P<0.05).ConclusionSomking can stimulate cell apoptosis and inflammatory response in nucleus pulposus cells via ESR pathway. Suppressing ESR may be a novel target to suspend smoking-induced intervertebral disc degeneration.
Lung cancer in never-smokers has been identified as a separate disease entity. Notably, the proportion of this distinct disease has been reported to increase in recent decades. Due to its occult onset and lack of clinical specificity, patients with this disease are always diagnosed with advanced stage. This review summarizes the current literatures about the risk factors, clinicopathological characteristics, molecular features, and prognosis of lung cancer in never-smokers, which will enhance our understanding and facilitate the precise management of this distinct disease.
ObjectiveThrough the analysis on outcome measurements in domestic and overseas randomized controlled trials (RCTs) of smoking cessation, this study aimed to provide references for clinical trial design in the future.
MethodsWe searched CNKI, WanFang Data, VIP, PubMed, EMbase, ScienceDirect and SpringLink databases to collect RCTs regarding smoking cessation from January 1998 to December 2013. Two reviewers screened literature according to the inclusive and exclusive criteria, extracted the data, and analyzed the outcome measurements of included RCTs.
ResultsA total of 68 RCTs regarding smoking cessation were included. As for the baseline measurements, the frequency from high to low were age, sex, daily cigarette, smoking duration, Fagerstrom Test For Nicotine Dependence (FTND), race and education, etc.; there were significant differences of race, education level, smoking duration, smoking, starting age of smoking, attempts of trying to stop smoking, the presence of other basic disease, FTND and quit date between English and Chinese RCTs (all P<0.05). As for efficacy measurements, the continuous abstinence rate (77.8%) was mainly adopted in Chinese RCTs, while point abstinence rate (95.1%) and continuous abstinence rate (82.9%) was selected in English RCTs. As for the follow-up measurements, 22.1% of the included RCTs did not report it, 70.6% of the RCTs reported abstinence rate, and the follow-up time in Chinese RCTs was shorter than that in the English RCTs (P<0.05).
ConclusionThe selection of outcome measurements is significantly different among RCTs regarding smoking cessation, the Chinese RCTs are inferior to English RCTs, and these are needed to be improved in the future clinical trials.
ObjectiveTo investigate the effects of smoking combined with intermittent hypoxia on the pathophysiology of lung tissue and thoracic aorta, and the endothelial injury.MethodsTwenty-four rats (SPF, female, six weeks old) were divided randomly into 4 groups (n=6). The control group was given false smoking and normal oxygen exposure, the smoking-exposed group was exposed in smoking, the intermittent hypoxia group was exposed in intermittent hypoxia environment, and the overlap group was exposed to smoking and intermittent hypoxia. After 8 weeks, body weight, right ventricular hypertrophy index (RVHI), the pathological changes of lung tissue and thoracic aorta were measured, and the level of endothelin-1 (ET-1), endothelial nitric oxide synthase (eNOS), vascular endothelial growth factor (VEGF) and stromal cell-derived factor-1α (SDF-1α) in serum of rats were evaluated.ResultsRVHI of rats in the smoking-exposed group, intermittent hypoxia group, overlap group were higher than that in the control group. In addition, RVHI in the overlap group was higher than that in the smoking-exposed group, intermittent hypoxia group (all P<0.05). The levels of ET-1, VEGF and SDF-1α in the serum of the smoking-exposed group, intermittent hypoxia group and overlap group were higher than those in the control group, while the level of eNOS was lower than that in the control group, (all P<0.05), the most significant difference was between control group and the overlap group. Pathological observation of lung tissue and thoracic aorta showed obvious emphysema in the smoking-exposed group and overlap group, which was more obvious in the overlap group than that in the smoking-exposed group (all P<0.05). Lung interstitial inflammatory infiltration, bronchial wall lymphocyte hyperplasia and pulmonary fibrosis were shown in different degrees in the smoking-exposed group, intermittent hypoxia group and overlap group, and the pulmonary arteriole wall showed thickening, fibrosis and peripheral inflammatory infiltration also were found in these groups. Thoracic aorta in the smoking-exposed group, intermittent hypoxia group and overlap group showed different degrees of endothelial cell injury, middle membrane thickening, and collagen fiber hyperplasia. The pathological features of the overlap group were most obvious compared to the other two groups.ConclusionsSmoking and intermittent hypoxia exposure can lead to different degrees of lung tissue and vascular endothelial injury and decrease of vascular endothelial protective factors in rats, resulting in dysfunction of vascular endothelial cells, which leads to the structural remodeling of pulmonary arterioles and aorta, such as thickening, fibrosis, etc. Combined smoking and intermittent hypoxia exposure can lead to more serious pathological damage.
Objective To investigate the effects of smoking on β-defensin-2 ( BD-2) expression in induced sputumand lung tissue, and its role in chronic obstructive pulmonary disease ( COPD) . Methods Patients suffering with early peripheral squamous celled lung cancer and underwent lobectomy were divided into a smoking COPD group ( COPD group) , a non-COPD smoking group ( smoker group) , and a nonsmoking group ( control group) . Preoperative induced sputumsamples were collected after hypertonic saline induction. Lung tissue samples were intraoperatively collected far from the tumor site. The sputum samples were prepared for total and differential cell count, while the lung tissue samples for pathology examination. The BD-2 concentration in sputumand lung homogenate were measured by ELISA. Correlation were analyzed between BD-2 concentration and smoking index, airway inflammation, and lung function. Results The lung pathology were highly consistent with the experimental grouping. The total cell count and neutrophils proportion in sputum and BD-2 concentration in lung homogenate were ( 2. 32 ±0. 51) ×106 / g, ( 35. 7 ±9. 8) % , and ( 14. 5 ±5. 7) ng/L in the control group respectively, while increased in the smoker group [ ( 4. 57 ±0. 87) ×106 / g, ( 52. 5 ±10. 9) % , and ( 78. 3 ±13. 1) ng/L, P lt;0. 05] , and further increased in the COPD group [ ( 6. 61 ±1. 03) ×106 / g, ( 65. 5 ±12. 3) % , and ( 127. 0 ±35. 0) ng/L, P lt; 0. 05] . The lymphocytes proportion and BD-2 concentration in sputum increased in the COPD group [ ( 3. 2 ±1. 7) % and ( 298. 0 ±135. 0) ng/L] as well as in the smoker group [ ( 2. 5 ±1. 2) % and ( 315. 0 ±124. 0) ng/L] ,as compared with the control group [ ( 1. 1 ±0. 3) % and ( 132. 0 ±48. 0) ng/L] ( P lt; 0. 05) . Linear correlation analysis revealed that BD-2 concentration in sputumwas positively correlated with smoking index,sputum total cell count and neutrophils proportion, whereas BD-2 concentration in lung homogenate wasreversely correlated with pulmonary ventilation function ( P lt; 0. 05) . Conclusions Smoking up-regulates the BD-2 level in sputum and lung tissues. Further more, the BD-2 expression status in lung tissue of smoking individuals might be associated with COPD susceptibility.
ObjectiveTo explore ways so as to improve smoking cessation rates by studying relevant cases in Hong Kong.MethodsPatients attending the clinical pilot project in Hong Kong from 2010 to 2022 were retrospectively surveyed and analyzed. Information such as patients' general information, reasons for smoking for the first time, situations that enable smoking, barriers to smoking cessation, and withdrawal symptoms were obtained using a pre-designed case report form and analyzed.ResultsA total of 10436 patients, 6936 males and 3500 females, were included. Influenced by friends (67.70%), relieving mental stress (33.12%) and curiosity (30.52%) were the main reasons for smoking for the first time; depression (57.14%), after meals (49.08%) and nervousness (41.26%) were the situations that enable smoking; the main barriers to smoking cessation were physiologic dependence (87.06%) friends or colleagues smoking (37.03%) and compulsiveness to use tobacco (32.45%), top withdrawal symptoms smoking stoppage were craving for cigarettes (50.33%), restlessness (38.33%), and difficulty concentrating (26.63%).ConclusionsThe proportion of patients actively choosing to quit smoking is high in Hong Kong, and smoking cessation methods should be publicized to prompt smokers to take effective measures to quit. A majority of people are influenced by friends to smoke for the first time; thus, adolescent smoking behavior should be supervised to reduce first-time smokers. Moreover, as the most difficult thing to overcome in the process of quitting smoking is psychological addiction, behavioral interventions must be promoted to improve the rate of successful quitting, Steps should be taken to enable the management of withdrawal symptoms to prevent relapse.
ObjectiveTo investigate the establishment of rat models with chronic obstructive pulmonary disease (COPD) combined with type 2 diabetes mellitus (DM).
MethodsEighty Sprague-Dawley (SD) male rats were randomly divided into four groups:COPD group (n=20), DM group (n=20), COPD combined with DM group (n=20) and normal group (n=20). COPD rats were established by cigarette smoke. Type 2 diabetes rats were modeled by streptozotocin injection. COPD combined with DM rats were modeled by cigarette smoking and streptozotocin injection at the same time. Pathological examination and blood glucose were tested after three months.
ResultsBronchial epithelium was seriously shedding in COPD+DM group, with alveolar structure damaged and some alveolar fused into bullae. The blood glucose level in COPD+DM group was (27.1±1.1) mmol/L, which was statistically different from other groups (P<0.05).
ConclusionRat model of COPD combined with type 2 DM could be established by cigarette smoking and streptozotocin injection, which can provide an animal model for further medical research.
ObjectiveTo systematically review the effectiveness and safety of bupropion for smoking cessation in smokers with cardiovascular disease.
MethodsDatabases including The Cochrane Library, PubMed, EMbase, Web of Science, CBM, CNKI, WanFang Data and VIP databases were electronically searched from inception to February 23rd, 2013. Randomized controlled trials (RCTs) on bupropion versus placebo for smoking cessation in smokers with cardiovascular disease were included. Two reviewers independently screened literature according to the inclusion and exclusion criteria, extracted the data, and assessed the methodological quality of included studies. Meta-analysis was performed by using RevMan 5.1 software.
ResultsIn total, 4 studies involving 1 415 patients were finally included. The results of metaanalyses indicated that, compared with placebo, bupropion significantly increased the point prevalence abstinence rate at 3 months (RR=1.79, 95%CI 1.14 to 2.83, P=0.01). However, the point prevalence abstinence rates at 6 months (RR=1.81, 95%CI 0.77 to 4.24, P=0.18) and 12 months (RR=1.46, 95%CI 0.94 to 2.27, P=0.10), and the continuous abstinence rates at 3 months (RR=1.48, 95%CI 0.89 to 2.47, P=0.13), 6 months (RR=1.41, 95%CI 0.79 to 2.51, P=0.25), and 12 months (RR=1.43, 95%CI 0.93 to 2.17, P=0.10) were similar in the two groups. The use of bupropion did not increase all-cause mortality (RR=1.13, 95%CI 0.49 to 2.56, P=0.78) and the incidence of cardiovascular events (RR=1.25, 95%CI 0.95 to 1.64, P=0.11).
ConclusionBupropion is safe to use in smokers with cardiovascular disease. Although bupropion could increase the point prevalence abstinence rate at 3 months, it is not effective for long-term smoking cessation. Due to the limited quantity and quality of the included studies, more large-scale high-quality RCTs are required to verify the aforementioned conclusion.
